Shallow breathing, decreased lung volumes,
and increased transpulmonary shunting as high as
20% of the cardiac output, are consistent
findings in most patients following major
operations. These alterations in pulmonary
function usually return to normal without
becoming clinically evident, but may progress to
obvious respiratory insufficiency with decreased
compliance, increased work of breathing, marked
shunting, retention of secretions, gross
consolidation, and pneurnonitis. The causes of
these phenomena are uncertain, but monotonous
tidal ventilation leading to alveolar closure
bas been shown to have this effect.

A maneuver which would assure voluntary
sustained maximal inspiration (SMI) with glottis
open, as in a prolonged yawn, should 1)
equilibrate ventilation and perfusion, and 2)
prevent alveolar atalectasis. An incentive
spirometer, which assured these conditions, was
constructed to test this hypothesis.

APPARATUS AND METHODS

As the subject inhales from the device, a
light turns on when he reaches a preset volume
(1/2 of the measured inspiratory capacity) and
stays on as long as an inspiratory flow rate of
50 cc./sec. is maintained. When total lung
capacity is reached, or if the subject closes
his glottis, the light turns off. The subject is
instructed to light the light as long as
possible by sustained maximal inspiration,
indeed, simulatinga yawn.

Pulmonary and hemodynamic studies were
carried out with a pneumotachograph flow and
volume system, inspired and expired gas control
and collection by one way valves, rapid nitrogen
and C02 analyzers, intravascular catheters for
pressure measuring and blood collection, and a
small intraesophageal pressure transducer. Five
normal volunteers and a series of postoperative
patients were studied to assess the changes
produced by this maneuver compared with other
respiratory maneuvers, and to observe the
effects of repeated SMI on pulmonary function in
postoperative patients.

RESULTS

During yawning (SMI) negative intrathoracic
pressure (-40 mm. Hg) was maintained throughout
inspiration causing sustained inspiratory flow
(average 200 cc./sec.) and increasing volume to
total lung capacity. Right atrial pressure
decreased (5 to -10 mm. Hg), mean pulnionary
artery pressure decreased (15 to 0 mm. Hg), and
venous return increased (measured by impedence
plethysmography). Cardiac output increased
slightly. ln healthy volunteers Pa O2 (air)
increased slightly (90 to 94 mm. Hg) as did Pa
O2 (l00% (580 to 596 mm. Hg), indicating that
ventilation perfusion relationships and shunt
were normal in these subjects and could not be
significantly improved. Arterial pCO2 and PH
were not affected by the maneuver. Rebreathing
or C02 breathing caused tachypnea with increased
tidal volume, giving effects qualitatively
similar to SMI but these effects were not as
marked and were not sustained. Cough, IPPB, a
held deep breath, blow boules, and other
positive pressure respiratory maneuvers produced
the hemodynamic effects of the Valsalva maneuver
with increased intravascular pressure, decreased
venous return, and decreased cardiac output. The
lung volume to which the subject inspired for
positive pressure maneuvers was generally far
short of total lung capacity.

ln ten postoperative patients with normal
preoperative pulmonary function, vital capacity
decreased to 60% of preoperative levels.
Alveolar arterial gradients for oxygen while
breathing 100% oxygen increased to 250 to 350
mm. Hg, corresponding to a 12% to 20% shunt. The
hemodynamic effects of SMI were the same as in
the normal volunteers. However, in the
postoperative patients ventilation/ perfusion
imbalance was demonstrated which could be
reversed by SMI. Pa 02 (air), increased from 70
to 94 mm. Hg. Alveolar-arterial gradient on l00%
02 was diminished by SMI [Pa 02 (100%) 440
to 520] suggesting opening of closed
alveoli. These effects were scen after five SMI
maneuvers. When this was repeated on an hourly
basis, the Pa 02 (room) and the Pa 02 (100%)
stayed at near normal levels. Unlike forced
exhalation, SMI is not painful in laparotomy
patients because only inspiratory muscles are
used, in fact patients accepted the incentive
spirometer enthusiastically. The device has also
been used to treat established atalectasis with
success and has been valuable in weaning
patients from prolonged ventilator
management.

Periodic SMI to total lung capacity can
prevent or reverse postoperative hypoxemia,
supporting the theory that alveolar atalectasis
due to shallow ventilation is one cause of
decreased lung volumes and shunt in
postoperative patients.

The beneficial effects on ventilation and
perfusion, and patient acceptance, suggest that
use of this device may decrease the incidence of
postoperative pulmonary complications, and
controlled clinical studies are underway.